南方医科大学学报 ›› 2012, Vol. 32 ›› Issue (11): 1548-.

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膜联蛋白A2在炎症性肠病肠粘膜中的表达及临床意义

张朝霞,赵芯梅,吕超蓝,李晨,智发朝   

  • 出版日期:2012-11-20 发布日期:2012-11-20

Annexin A2expression in intestinal mucosa of patients with inflammatory bowel disease and its clinical implications

  • Online:2012-11-20 Published:2012-11-20

摘要: 摘要:目的探讨膜联蛋白A2(ANXA2)在炎症性肠病(IBD)肠粘膜组织中的表达及临床意义。方法免疫组织化学、荧光定量
PCR方法检测ANXA2在54例溃疡性结肠炎(UC)、37例克罗恩病(CD)及15例正常肠粘膜组织中的表达,并分析其表达与IBD
临床、病理及内镜参数间的关系。结果ANXA2在UC的阳性表达显著高于CD及正常对照组(P<0.05),且UC中临床表现严
重、内镜分级高的患者较临床表现轻、内镜分级低者表达显著升高(P<0.05)。ANXA2在CD的表达较正常对照组低(P<0.05),
其表达与CD的临床病理参数无相关性(P>0.05)。与正常对照及CD相比较,ANXA2mRNA表达量在UC中明显升高(P<
0.05)。结论ANXA2可作为IBD的诊断与鉴别诊断指标,ANXA2表达在UC发生发展中可能起着重要作用,有望作为其早期
诊断及靶向治疗的分子标记。

Abstract:
Objective To explore the role of annexin A2(ANXA2) expression in the intestinal mucosa in the pathogenesis of
inflammatory bowel disease (IBD).MethodsIntestinal or colonic mucosal biopsy samples were obtained from54patients with
ulcerative colitis (UC),37with Crohn’s disease (CD), and15healthy control subjects. Immunohistochemistry was employed to
examine the expression of ANXA2in the intestinal mucosa, and mRNA expression of ANXA2was detected using real-time
PCR.ResultsImmunohistochemistry showed a ANXA2positivity rate of83.3% (45/54) in patients with UC, 27.0% (10/37) in
patients with CD, and53.3% (8/15) in the control subjects. ANXA2 expression in the intestinal or colonic mucosa was
significantly up-regulated in patients with UC compared with the patients with CD and healthy control subjects, but was
significantly lower in patients with CD than in the healthy controls (P<0.05). The expression levels of ANXA2were strongly
associated with the severity of clinical manifestations and the histopathological grades of UC (P<0.05). Compared with the
healthy controls and patients with CD, patients with UC showed a significantly increased ANXA2mRNA expression level in
the inflamed mucosa of UC (P<0.05). ConclusionANXA2can serve as a marker for differential diagnosis of IBD, and its
up-regulated expression is closely related to the pathogenesis of UC.